(TBI) is one of the most common neurological disorders in the United States with the majority of the cases being classified as mild injury (GCS 13-15). Although diffuse axonal injury (DAI) may be present among such patients, it is often missed by CT and conventional MRI. This disruption of white matter connections between disperse regions of the brain will likely disrupt the large-scale neural networks supporting cognition. Therefore, in spite of being labeled as acquiring only mild injuries, many of these individuals suffer from cognitive symptoms, including memory complaints, as long-term sequelae from the injury. Functional MRI is a useful tool for assessing such disturbances in large-scale neural networks. Through resting state fMRI, groups have demonstrated a number of functionally connected neural networks including the default mode network (DMN) (TPN). During a working memory task, the DMN is suppressed while the TPN is activated. The Default Mode Interference Hypothesis suggests that the efficient switching between these two networks is required for peak cognitive performance. Further, if the TPN fails to adequately deactivate or suppress the activity of the DMN, there is an interference with goal directed behavior represented as a lapse in attention. This lapse in attention can be represented behaviorally by an increased reaction time or increased variability in reaction time throughout the duration of a task. The DMN and TPN are ideally anti-correlated as demonstrated by negative functional connectivity between the two networks. Due to the diffuse nature of the injuries associated with mTBI, we hypothesize that working memory deficits experienced after mTBI are associated with altered modulation of the interactions between the DMN and the TPN. A greater degree of disruption between these two networks will be associated with poorer performance on working memory tasks. I will test this hypothesis using fMRI of the N-back working memory paradigm in the sub-acute stage of mild TBI. I will assess patterns of neural activity in the DMN and the TPN during the working memory task. In addition, I will assess functional connectivity between the DMN and TPN during both rest and the working memory task. Results from this study will for the first time elucidate the neural correlates and mechanisms for lapses in working memory stemming from mild traumatic brain injury